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G.J. Ben Simon, N.G. Harris, F. Gomez–Pinilla, D. Hovda, R.A. Goldberg; Traumatic Optic Neuropathy in a Rat Model – The Effect of Traumatic Brain Injury (TBI) on Retinal Ganglion Cells (RGCs) Survival After Optic Nerve Crush, and the Role of Brain Derived Neurotrophic Factor (BDNF) in Immune Mediated Neuroprotection . Invest. Ophthalmol. Vis. Sci. 2005;46(13):666.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To study the effect of traumatic brain injury (TBI) on retinal ganglion Cells (RGCs) survival after optic nerve crush in a rat model for traumatic optic neuropathy. To evaluate the role of retina brain derived neurotrophic factor (BDNF) on immune mediated neuroprotection. Methods: Male Sprague–Dawly rats were exposed to optic nerve crush at different time intervals after traumatic brain injury (TBI) to the contralateral brain hemisphere. Retinal ganglion cells (RGCs) survival was assessed two weeks after crush injury by counting the RGCs retrogradely labeled with 4–(4–(didecylamino)– styryl)–N–methylpyridinium iodide (4–Di–10–Asp). The experiment will be repeated for measurements of BDNF in the rats’ retina and for evaluation the effect of systemic steroids (methyl–prednisolone) on the possible neuroprotective effect of TBI. Results: Optic nerve crush injury resulted in RGCs death in a dose–response manner. Mild crush resulted in 20% death while moderate to severe crush resulted in up to 50% RGCs death two weeks after the injury. Traumatic brain injury is anticipated to cause immune–mediated neuroprotection and to salvage dying RGCs if performed 1–2 weeks prior to optic nerve crush but not concomitantly with the crush. The neuroprotective effect is likely to parallel BDNF levels in rats’ retina and is believed to be immune mediated. Systemic steroids are believed to alleviate the anticipated neuroprotective effect. Conclusions: Traumatic brain injury at a distant site may have a neuroprotective effect on RGCs survival after optic nerve crush, this is believed to be, at least in part, secondary to an increased BDNF levels at the injury site and may be immune mediated.
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